To extend studies concerning serum and spinal fluid complement components in patients with central nervous system manifestations of S.L.E. including an analysis of participation of the alternate pathway of complement activation by measurement of serum levels of the C3 proactivator. Further, to demonstrate conclusively in vivo activation of complement in the CSF by documenting the presence of reaction products of complement components (e.g., alpha2D, C3b, or C4i) or activated components (e.g. Cl) in CSF. Another means of documenting complement activation will be to measure other complement properties within the CSF and to compare such complement profiles with serum profiles indicative of activation of the classic or alternate pathway. Secondly, to investigate abnormalities of spinal fluid complement in neuropsychiatric disorders other than S.L.E. Assays of complement components and an attempt to demonstrate reaction products or activated components will be carried out. Third, to extend previous studies from our laboratory concerning the in vivo metabolism of C3 in human disorders. Fourth, to study the quantitative immunology of red cell sensitization with complement components in acquired hemolytic anemias in order to correlate such quantitation with clinical findings and with serologic reactions to further clarify the role of complement in immune red cell destruction. Methods used will be the use of hemolytic assays and immunochemical techniques; immunodiffusion, electrophoresis in antibody containing gels and radioimmunoassay. The in vivo kinetics of radiolabelled, purified complement proteins will be studied to determine catabolic and synthetic rates. Finally, a sensitive new immunochemical method based on antigen inhibition of lysis of complement sensitized sheep cells will be used to study the significance of in vivo red cell bound complement components.